Department of Bioscience and Bioengineering, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India.
Int J Cancer. 2024 Aug 15;155(4):605-617. doi: 10.1002/ijc.34991. Epub 2024 May 8.
Glioblastoma (GBM) is one of the most lethal malignancies in humans. Even after surgical resection and aggressive radio- or chemotherapies, patients with GBM can survive for less than 14 months. Extreme inter-tumor and intra-tumor heterogeneity of GBM poses a challenge for resolving recalcitrant GBM pathophysiology. GBM tumor microenvironment (TME) exhibits diverse heterogeneity in cellular composition and processes contributing to tumor progression and therapeutic resistance. Autophagy is such a cellular process; that demonstrates a cell-specific and TME context-dependent role in GBM progression, leading to either the promotion or suppression of GBM progression. Autophagy can regulate GBM cell function directly via regulation of survival, migration, and invasion, or indirectly by affecting GBM TME composition such as immune cell population, tumor metabolism, and glioma stem cells. This review comprehensively investigates the role of autophagy in GBM pathophysiology.
胶质母细胞瘤（GBM）是人类最致命的恶性肿瘤之一。即使经过手术切除和积极的放疗或化疗，GBM 患者的存活时间也不到 14 个月。GBM 的极端肿瘤内和肿瘤间异质性给解决难治性 GBM 病理生理学带来了挑战。GBM 肿瘤微环境（TME）在细胞组成和促进肿瘤进展和治疗耐药的过程方面表现出多样化的异质性。自噬就是这样一个细胞过程；它在 GBM 进展中表现出细胞特异性和 TME 上下文依赖性作用，导致 GBM 进展的促进或抑制。自噬可以通过调节生存、迁移和侵袭直接调节 GBM 细胞功能，或者通过影响 GBM TME 组成，如免疫细胞群体、肿瘤代谢和神经胶质瘤干细胞来间接影响 GBM 细胞功能。本综述全面研究了自噬在 GBM 病理生理学中的作用。
